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PubMed2003

CD4+ T cells mediate IFN-gamma-independent control of Mycobacterium tuberculosis infection both in vitro and in vivo.

Although IFN-gamma is necessary for survival of Mycobacterium tuberculosis infection in people and animal models, it may not be sufficient to clear the infection, and IFN-gamma is not a reliable correlate of protection. To determine whether IFN-gamma-independent mechanisms of immunity exist, we developed a murine ex vivo culture system that directly evaluates the ability of splenic or lung lymphocytes to control the growth of M. tuberculosis within infected macrophages, and that models in vivo immunity to tuberculosis. Surprisingly, CD4(+) T cells controlled >90% of intracellular M. tuberculosis growth in the complete absence of IFN-gamma stimulation of macrophages, via a NO-dependent mechanism. Furthermore, bacillus Calmette-Guerin-vaccinated IFN-gamma-deficient mice exhibited significant protection against M. tuberculosis challenge that was lost upon depletion of CD4(+) T cells. These findings demonstrate that CD4(+) T cells possess IFN-gamma-independent mechanisms that can limit the growth of an intracellular pathogen and are dominant in secondary responses to M. tuberculosis.

Administration, Inhalation↗
PubMed2006

NK cell-derived IFN-gamma differentially regulates innate resistance and neutrophil response in T cell-deficient hosts infected with Mycobacterium tuberculosis.

Although it is known that IFN-gamma-secreting T cells are critical for control of Mycobacterium tuberculosis infection, the contribution of IFN-gamma produced by NK cells to host resistance to the pathogen is less well understood. By using T cell-deficient RAG(-/-) mice, we showed that M. tuberculosis stimulates NK cell-dependent IFN-gamma production in naive splenic cultures and in lungs of infected animals. More importantly, common cytokine receptor gamma-chain(-/-)RAG(-/-) animals deficient in NK cells, p40(-/-)RAG(-/-), or anti-IFN-gamma mAb-treated RAG(-/-) mice displayed significantly increased susceptibility to M. tuberculosis infection compared with untreated NK-sufficient RAG(-/-) controls. Studies comparing IL-12 p40- and p35-deficient RAG(-/-) mice indicated that IL-12 plays a more critical role in the induction of IFN-gamma-mediated antimycobacterial effector functions than IL-23 or other p40-containing IL-12 family members. The increased susceptibility of IL-12-deficient or anti-IFN-gamma mAb-treated RAG(-/-) mice was associated not only with elevated bacterial loads, but also with the development of granulocyte-enriched foci in lungs. This tissue response correlated with increased expression of the granulocyte chemotactic chemokines KC and MIP-2 in NK as well as other leukocyte populations. Interestingly, depletion of granulocytes further increased bacterial burdens and exacerbated pulmonary pathology in these animals, revealing a compensatory function for neutrophils in the absence of IFN-gamma. The above observations indicate that NK cell-derived IFN-gamma differentially regulates T-independent resistance and granulocyte function in M. tuberculosis infection and suggest that this response could serve as an important barrier in AIDS patients or other individuals with compromised CD4+ T cell function.

Animals↗
PubMed2000

Disseminated histoplasmosis with reactive hemophagocytosis: aspiration cytology findings in two cases.

Two cases of disseminated histoplasmosis associated with reactive hemophagocytic syndrome are described. The clinical presentation was with prolonged unexplained fever and hepatosplenomegaly. On a strong clinical possibility of tuberculosis, antitubercular treatment was initiated in both patients. Lymph node (case 1), splenic (case 2), and bone marrow aspiration, however, showed sheets of proliferating histiocytes, and intracellular and extracellular histoplasma organisms. Aspiration cytology was thus valuable in establishing the final diagnosis. The patients had a fulminant clinical course and died of hemorrhagic shock within 48 hr of hospital admission before specific therapy could be initiated. Histoplasmosis can mimic tuberculosis clinically. There is a need for an increased awareness of the clinicopathological spectrum of histoplasmosis, especially its rarer manifestations as hemophagocytic syndrome. In suspected cases, aspirations from the lymph node, liver, and spleen can be performed safely and should be utilized for early diagnosis.

Adult↗
PubMed1981

Several conditions causing elevation of serum CK-MB and CK-BB.

Most of the creatine kinase (CK:EC 2.7.3.2) activity is present in skeletal muscle and myocardium. However, some activity in other organs has been reported. Theoretically, the destruction of organs that contain CK activity should release soluble enzymes into the general circulation. The effects of various destructive processes on serum creatine kinase isoenzymes in 70 patients were studied. The MB isoenzyme was demonstrated in 17 of 70 patients (24%), and the BB isoenzyme in 12 of 70 patients (17%). MB activity ranged from 3 to 12 U/l, or 0.7% to 10% of the total CK activity. BB activity ranged from 2.5 to 21 U/l, or 0.4% to 18.6% of the total CK activity. Interpretation of the results of CK isoenzyme studies should be made very carefully, especially if laboratories use CK-MB methods that measure MB and BB in combination. The diagnosis of myocardial injury should never be based solely on the presence of creatine kinase MB isoenzyme in the serum, but should be supported by additional clinical and laboratory data.

Adolescent↗
PubMed1997

Evidence of differential mycobacterial growth and modulation of mycobactericidal property by glucoaminylmuramyl dipeptide in murine macrophages.

These results show that given a source of mouse tissue macrophage, there is differential mycobacterial growth with different species of mycobacteria. This suggests that each species of mycobacteria generates a differential response in a given tissue macrophage within the same host for its survival. For example, BCG-P growth becomes permissive in the presence of GMDP in splenic and peritoneal macrophages. Whereas in the same tissue M. tuberculosis growth becomes non-permissive. From Table 2 it is evident that inhibition of inflammatory responses following M. tuberculosis infection leads to reduction of viable organisms in murine macrophages.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1985

Killed Listeria-induced suppressor T cells involved in suppression of delayed-type hypersensitivity and protection against Listeria infection.

Pretreatment of mice by intravenous injection with killed Listeria provided neither delayed-type hypersensitivity to Listeria protoplasm nor protection against Listeria infection. Assuming that this suppression is due to suppressor cells, we attempted to clarify their induction and characterization. Pretreatment with killed BCG instead of killed Listeria suppressed the induction of DTH and protection in subsequent Listeria-immunized mice. Conversely, pretreatment with killed Listeria suppressed subsequent induction of DTH to PPD or protection from tuberculosis. Thus, these suppressions were induced antigen nonspecifically. Transfer of splenic non-adherent cells from killed Listeria-injected mice which had been treated with anti-BA theta serum plus complement, or had been passed through Sephadex G-10 columns, resulted in both afferent and efferent DTH suppression, suggesting that the DTH suppression is closely associated with suppressor T cells. Moreover, the splenic nonadherent cells from killed Listeria-injected mice showed suppression in vitro of listericidal activity of PEC from Listeria-immune mice in the presence of Listeria protoplasm.

Animals↗
PubMed2002

Florid pulmonary inflammatory responses in mice vaccinated with Antigen-85 pulsed dendritic cells and challenged by aerosol with Mycobacterium tuberculosis.

Mice immunized by the intranasal route with dendritic cells harvested from the lungs and then pulsed with Ag85 (LDC-Ag85) were able to prime naive CD4(+) T cells in vivo. As a result splenic CD4(+) T cells from these immunized mice were able to produce IFNgamma following culture with Mycobacterium tuberculosis-infected antigen presenting cells. Hematoxylin and eosin stained lung sections from LDC-Ag85 immunized mice after they had been exposed to aerosol challenge with M. tuberculosis showed a florid infiltration of macrophages and lymphocytes into granulomas and parenchymal tissues when compared to lung sections from control groups implanted with dendritic cells pulsed with ovalbumin. In addition, using immunohistochemistry, these tissues appeared to have more CD4(+) and CD8(+) cells than the control groups. This was confirmed by flow cytometric analysis which showed that lung cell digests contained increased numbers of CD4 and CD8 interferongamma secreting cells. Despite this increase however, no evidence was seen that indicated that the LDC-Ag85 immunized mice were more resistant to M. tuberculosis infection than mice immunized with LDC pulsed with an irrelevant protein. Instead, the potent inflammatory response in the LDC-Ag85 resulted in serious consolidation of the lung tissue.

Acyltransferases↗
PubMed1998

Vaccination with plasmid DNA encoding mycobacterial antigen 85A stimulates a CD4+ and CD8+ T-cell epitopic repertoire broader than that stimulated by Mycobacterium tuberculosis H37Rv infection.

Vaccination of mice with plasmid DNA carrying the gene for the major secreted mycobacterial antigen 85A (Ag85A) from Mycobacterium tuberculosis is a powerful technique for generating robust specific Thl helper T-cell responses, CD8+-mediated cytotoxicity, and protection against M. tuberculosis challenge (K. Huygen et al., Nat. Med. 2:893-898, 1996). We have now analyzed in more detail the antigen-specific immune CD4+- and CD8+-T-cell responses induced in BALB/c mice vaccinated with Ag85A DNA and have compared these responses to those generated by intravenous infection with M. tuberculosis. T-cell-epitope mapping, as measured by interleukin-2 and gamma interferon secretion from splenic T cells restimulated in vitro with synthetic 20-mer peptides spanning the complete mature sequence of Ag85A, demonstrated that DNA vaccination stimulated a stronger and broader T-cell response than did M. tuberculosis infection. Moreover, elevated cytotoxic T lymphocyte (CTL) activity against Ag85A-transfected and peptide-pulsed P815 target cells could be generated exclusively by vaccination with plasmid DNA, not following M. tuberculosis infection. By using DNA vaccination, three Ag85A CTL epitopes with predicted major histocompatibility complex class I binding motifs were defined. One of them was previously reported as a dominant, promiscuously recognized T-cell epitope in healthy humans with primary infections. These data strengthen the potential of DNA vaccination with respect to inducing antituberculous immunity in humans.

Amino Acid Sequence↗
PubMed1987

[Pseudotumorous liver tuberculosis with multiple organ abscesses. A contribution to the differential diagnosis of liver abscess].

In a patient hospitalized with the diagnosis "fever of unclear etiology", a large liver abscess with multiple organ abscesses (soft tissues of the throat, spleen) was found. The bacteriological investigation of the liver abscess punctation material and the histological investigation of material from a throat abscess did not lead to a diagnosis. The causative organism was only detected by a specific investigation for M. tuberculosis (bacteriological, ELISA). Apart from one exception, there has been no reference to the possible causation of large liver abscesses by M. tuberculosis in the review literature in this country and abroad. In the case described, the tuberculous liver abscess was caused to regress by pharmacotherapy.

Abscess↗
PubMed1981

Production of a suppressor factor by adherent cells from Mycobacterium tuberculosis-infected guinea-pigs.

Adherent cells from the spleen of guinea-pigs infected with Mycobacterium tuberculosis (M. tuberculosis) spontaneously released a factor which suppressed the blastogenic response of normal guinea-pig and human peripheral blood lymphocytes to PHA activation. Suppressor factor production was evident within 3 hr of culture, continued for 2 days and diminished thereafter. This effect was not observed in supernatants derived from normal guinea-pig splenic adherent cells or from peripheral blood adherent cells of both normal or M. tuberculosis-infected guinea-pigs. Analysis of the spontaneously generated adherent cell supernatant indicated that it activated a subpopulation of lymphocytes to become suppressor cells. We conclude that adherent cells phagocytosing M. tuberculosis at the site of the lesion release a factor which activates suppressor cells, and that these cells may be important in the cellular unresponsiveness which develops in animals or man with advanced tuberculosis.

Animals↗
PubMed2004

Combined DNA vaccines formulated in DDA enhance protective immunity against tuberculosis.

This study evaluated the adjuvant Dimethyldioctyldecyl Ammonium Bromide (DDA) effect on the protective immunity induced by a combination of plasmids containing genes encoding antigens Ag85B, MPT-83, and ESAT-6 from Mycobacterium tuberculosis. The combined DNA vaccines in DDA resulted in significant increases in both specific IgG and splenic T-cell-derived Th1-type cytokine gamma interferon (IFN-gamma) production in response to the three purified antigens when compared to that of combined DNA vaccines in saline. Vaccines in DDA increased the protective efficacy of mice challenged with M. tuberculosis H37Rv as measured by reduced relative CFU counts in their lungs. Mice immunized with the combined DNA vaccines were shown to limit the growth of tubercle bacilli both in lungs and in spleens. Histopathological analyses showed that vaccinated mice had substantially improved postinfection lung pathology relative to the controls. We suggest that our combination of antigens together with DDA formulation may provide a new insight into tuberculosis prevention.

Acyltransferases↗
PubMed1973

Relationship between tuberculin hypersensitivity and cellular immunity to infection in mice vaccinated with viable attenuated Mycobacterial cells or with Mycobacterial ribonucleic acid preparations.

The migration inhibition technique has been used to study delayed hypersensitivity in vitro by using peritoneal exudate cells and splenic lymphocytes from mice vaccinated with viable cells of the attenuated H37Ra strain of Mycobacterium tuberculosis and from mice vaccinated with ribonucleic acid (myc RNA) preparations obtained from viable mycobacterial cells of the same strain. Inhibition of macrophage migration was noted when purified protein derivative (PPD) or viable H37Ra cells were added to peritoneal exudate cells obtained from mice immunized with viable H37Ra cells and not from mice immunized with myc RNA. Splenic lymphocyte cultures were exposed to the same antigens in vitro. Filtered supernatant fluids from these lymphocyte cultures, when added to peritoneal exudate cells obtained from nonimmunized mice, inhibited migration only when they were obtained from lymphocytes which came from mice immunized with viable H37Ra cells. Injection of PPD intravenously into vaccinated mice resulted in inhibitory supernatant fluids from splenic lymphocyte cultures only when the lymphocytes came from mice immunized with viable H37Ra cells. However, intravenous injection of either viable H37Ra cells or of myc RNA preparations into mice vaccinated with myc RNA occasionally produced inhibitory supernatant fluids when lymphocytes were obtained from these mice. On the other hand, mice vaccinated with myc RNA or viable H37Ra cell preparations were consistently and equally protected against intravenous challenge with the virulent H37Rv strain. Thus, although some evidence was obtained for a delayed type hypersensitivity in mice vaccinated with H37Ra cells or with myc RNA to ribosomal proteins or other proteins associated with the RNA preparation, no evidence of tuberculin hypersensitivity could be detected in any mice vaccinated with the myc RNA. These results argue against a role for tuberculin hypersensitivity in immunity to tuberculous infection.

Animals↗
PubMed1991

[Splenic abscess: clinico-microbiologic study of 15 cases].

We have reviewed 15 cases of splenic abscesses diagnosed using a histopathological and microbiological study. Mean age was 48 years (range 18-78). Eight of them were male and 7 female. Eighty per cent of them had predisposing diseases, amongst which the most frequent were endocarditis and bacteriemia of other origin (26.6% in both cases). All patients presented fever and in 7 of them (47%) splenomegaly was appreciated. The most frequently isolated germs were gramnegative bacteria (33%), anaerobics (20%), and with a similar incidence grampositive bacteria, tuberculosis and fungii; in only one case cultures were sterile. Seven patients had multiple splenic abscesses and 8 patients single abscesses. Thorax x-ray showed alterations in more than half of the patients (53%). Abdominal echography was the diagnostic method in 67% of the patients and TAC in all the cases in which it was performed. Eight patients underwent splenectomy and one was surgically drained being the mortality rate of this group of 22%. Overall mortality was 33% and was related to the presence of multiple splenic abscesses (5/7, 71.4%), positive hemocultures (6/6, 100%), extrasplenic abscesses (7/8, 87.5%), and endocarditis (4/4, 100%), fungii infections (2/2, 100%), and late diagnosis (6/6, 100%).

Abscess↗